Shared Errors in the DNA of Humans and Apes

David A. Plaisted

It has been claimed that there are shared "errors" in the DNA between
humans and apes, and that this shows that humans and apes must have a
common ancestor, because the Lord would not have inserted common
errors in their DNA. These errors are generally in the form of
pseudogenes, which are genes that have lost their function for some
reason, often because control sequences around them are not present.
Here are some thoughts about these shared "errors" in DNA. The
following material has extensively been modified since Edward Max's
first response to it.

1. At first glance, this appears to be a strong argument for
evolution. Indeed, I found it troubling for a while.

2. However, we are still learning, and it is hard to know when a part
of the DNA is beneficial or harmful. How do we know for sure what is
an error? Even the so-called junk (nonfunctional) DNA may have a
function that we do not yet understand. For example, an article in
Science (4 April 1997, page 39) suggests that "satellite DNA," which
some researchers regard as nonfunctional, may have a function. See
also Science 1994, Feb 4 pp. 608-610. This whole area is sufficiently
new that it is best to wait a little longer. We should also look at
shared properties of the DNA between many species, and see if they can
consistently be placed in an evolutionary tree. If not, then this
calls into question the human-ape connection.

3. Mutations are not completely random. It's possible that the same
kinds of mutations tend to occur in the same way (for example, where
the DNA folds, or whatever. Dan Hughes also suggests that DNA might
tend to adopt a low energy state.) This could explain many common
errors. Note that mutations in a population can be expected to obey
more regularities than those among individuals, because of the
similarities in survival benefits and the laws of large numbers.

4. Maybe the Lord inserted those similarities for a reason we do
not understand. They could even have been inserted as tests of
our faith. The Lord does not force any to believe, but gives
opportunity to doubt for those who are seeking it.

5. Another possibility is that the Lord, when he cursed Adam and Eve
after the fall, also cursed all life by introducing errors into the
DNA. One could expect that similar species were cursed in a similar
way, out of fairness.

6. Edward Max's argument is based on the fact that these shared
sequences are really errors, that is, mistakes. It seems strange to
call something an "error" when it occurs in a nonfunctional part of
the DNA. Since that part of the DNA is nonfunctional, it doesn't
matter what occurs there, so there is no justification for calling
some of the sequences errors.

7. Something has to appear in the nonfunctional part of the DNA. Why
should it be one thing rather than another? Just by chance (accident)
there are likely to be sequences that resemble genes, but this says
nothing about their origin. Do we expect that the Lord would have
deliberately avoided common subsequences at common locations just so
that we would not think there was common descent?

8. Let us consider humans and apes. Since they are so similar, one
would expect that they had many similar genes at the creation in
similar locations in the genetic material. Also, with the change in
environment since then, one would expect that some of these genes
would no longer be necessary, such as the gene for synthesizing
vitamin C, and that there would be a few such genes in common between
apes and men. Now, point mutations arise all the time, and if they
are fatal or harmful, they will disappear from the population (have a
small frequency). If they are neutral, they can be passed on. So it
is reasonable that point mutations inactivating the vitamin C
synthesizing genes would occur in both humans and apes, and be
preserved in both, since these genes have little benefit now. Thus we
would get a pseudogene in the same location in humans and apes. It
could have been present in the individuals on the ark, for example.
This probably would occur for a few other genes, as well. For
organisms that are less similar, this still could happen, but less
often. So we would expect to find a pattern of common pseudogenes
that reflects the similarity between organisms, but not as an evidence
of common descent.

Actually, the LGGLO pseudogene (an inactivated Vitamin C synthesis
gene) has been found in one human so far and no apes, according to
Edward Max, but in his essay he predicts that it should be found in
apes, too. In fact, given the similarity in the DNA of humans and
apes, that is a reasonable prediction. There are other examples of
common pseudogenes that he says have been found in humans and apes,
but I do not know yet if they occur in exactly the same form in humans
and apes, or in how many individuals they have been found, or how many
base pairs they have. Even if they do occur in the same form, this
would be a problem for evolutionary theory, I think, because neutral
mutations tend to be eliminated from populations, according to the
talk.origins archive, and one would not expect a neutral mutation to
persist for so long. Some neutral mutations can spread to the whole
population, but this generally takes a very long time and has a low
probability. (The chance that this will happen is proportional to the
frequency of a neutral mutation in the population.) By seeing how
much variation exists between copies of the mutated region in
different organisms, one could estimate its time of origin and in this
way check evolutionary timetables, since non-functional DNA probably
mutates at constant rates. One would not expect to find a large
number of shared neutral mutations among all humans and apes, in any
event. Also, one would expect to find neutral mutations that had only
spread to half or a fourth of the population, too, since they spread
so slowly when they do spread. Furthermore, one would expect a gene
to be inactivated in many different ways, so that exactly the same
form should not be found today in all individuals. This would seem to
imply a very severe population bottleneck at some time in the past.

9. It is even possible that the lack of ability to synthesize vitamin
C could be an advantage in certain situations, although this appears
unlikely. It could be that individuals without this ability would be
forced to move to a different location, and this new location could
turn out to be a more favorable habitat. The same could be true for
the loss of some other genes.

10. Before being created, life was an idea in the mind of God. The
relationship between the created life forms reveals something about
how ideas develop in the Divine mind. We cannot say in advance how
these ideas develop, which makes it difficult to draw conclusions
about how the various life forms were interrelated at the creation.

By the way, concerning the junk DNA, it should also be mentioned that
this DNA helps to concentrate certain kinds of mutations (crossovers,
recombinations) at certain places in a protein molecule, and this can
be a valuable function. The recombinations are likely to occur
between the pieces of a gene, and not in the midst of it. This could
have a useful function. However, this should only be dependent on the
length of the junk sequence, and not its content.

The talk.origins site about this subject is carefully reasoned and
does a fairly good job of presenting the creationist side, by the way,
although it becomes somewhat biased and sarcastic at the end, in my
opinion.

I wanted to comment in more depth about the effects of the curse. One
of the purposes of the Creation is to illustrate spiritual truth.
Before the entrance of sin, a perfect creation could faithfully
represent spiritual reality. After the fall of man, this was no
longer so. Now it would be necessary for the plants to bear thorns
and thistles to teach spiritual lessons, and for the soil to be
difficult to work. Jesus in his parables often referred to the things
of nature as illustrations of the workings of good and evil. It is
sad that the innocent animals had to bear the effects of sin which
they had not caused, but their sufferings do help to bring to the mind
of man the terrible effects of evil and lead him back to God.

Shared Errors and Rates of Evolution

It is interesting that the existence of shared errors in DNA allows us
to estimate rates of evolution, because it permits us to put a rough
bound on the population size. We will make some calculations on this
basis. Of course, there are many assumptions, so these calculations
are not conclusive, but they may be of some general interest
anyway.

The key observation is that according to population genetics, if a
neutral mutation spreads to a population of size N, it takes an
average of 4N generations to do it. So if we see a number of neutral
mutations spread to the whole population in M generations, this
suggests that the average population size since the neutral mutations
was at most about M/4.

Now, let's consider the time since the Cambrian explosion about 570
million years ago, and consider the assumed evolutionary ancestors of
man during this time. This is about 5 * 10 8 years. We
can estimate an average generation time of at least half a year; even
if organisms can reproduce faster, a typical individual will be born
after more than one reproductive cycle. This gives about 10 9
generations. Suppose that we find shared pseudogenes going
back all the way to the beginning of the Cambrian explosion but not
much farther. These would have spread to the whole population in
109 generations, implying an average population size of
about 2.5 * 108. Now, we can also assume that shared
pseudogenes will be found from later periods, which would have had to
spread correspondingly faster. This implies that the average
population size was decreasing with time, so we can say that about
1.25 * 108 is a reasonable value, which we round to
108. Humans have about 3 * 109 base pairs in
the genetic material, which has been increasing in length. Thus its
average length would probably be less than 2 * 109. Thus
there would be about 2 * 1017 base pairs per generation.
The rate of mutation is estimated to be one in 1010 to one
in 1012 base pairs per generation. Let's use one in
1011. This means 2*106 mutations per
generation.

We distinguish between major and minor mutations, as explained in A Theory of Small Evolution.. A major
mutation is one that changes the shape of a protein. This would
include increasing its length. Now, of 2*106 mutations per
generation, maybe 9/10 would occur in the nonfunctional region,
leaving 2*105 in the functional region per generation. Of
these probably half would be minor mutations or have no effect at all
and the other half would change the shape of a coded protein, giving
105 major mutations per generation.

Now, we estimate the probability that a protein with a changed shape
will have a beneficial function in the organism. In reality this
appears to be vanishingly small, but we will be very generous. In the
immune system, it generally takes about 100,000 antibodies before one
is found that binds to an invading organism (antigen). This is a
highly specialized system, and a protein generally has to do more than
just bind to something in order to be beneficial, so we will say one
in 106 major mutations is beneficial. From 105
major mutations in all, this implies that about 1/10 per generation
are beneficial. Even most beneficial mutations do not fix (reach a
frequency near one) in the population, so we will assume that 1/100 of
these fix, leading to 1/1000 per generation that fix. In
109 generations, this leads to 106 beneficial
major mutations that fix.

Actually, the one in 106 figure is much too high because
antibodies all have the same shape, roughly speaking. Proteins have
many different shapes, and these also must match precisely for the
proteins to interact. It takes a lot of information to specify a
three-dimensional shape, so we can say that the probability is one in
106 that the shape will be right for an interaction. The
protein also has to be able to "unstick" from its partner at the right
time; this requires a carefully constructed system, and we will say
another probability of one in 106 for this. This leads to
a probability of one in 1018 so far to interact with one
other protein. Generally a protein has to interact with at least 2
others, so we can square this to obtain one in 1036. Now,
even if a protein interacts, in all probability this will be a harmful
interaction, so we can say that the chance of a beneficial interaction
is much less than one in a thousand, leading to a probability of one
in 1040 overall. This agrees with the fact that the
smallest genes typically have about 150 base pairs, and
4150 is about 1090. If this (admittedly
approximate) one in 1040 figure is anywhere correct, then
the probability of a single beneficial major mutation in the history
of human evolution is essentially nil.

Let us consider in more detail the mutations that add a base pair to a
gene. If this is added in the middle, it will probably change the
shape of the gene significantly; especially will several such
mutations in the middle have this effect. Now, a mutation at the end
might just tack on a new amino acid to the polypeptide sequence but
not change its shape. Each gene is composed of pieces, an average of
three pieces, each typically in length from 50 to 1000 amino acids,
that is, 150 to 3000 base pairs. Let's use 1000 as a typical value.
An addition of a base pair in the middle of a piece will mess up the
3-base pair codons terribly and produce a completely new protein with
a new shape. The chance that a mutation will occur at the end of this
sequence is about one in 1000, among those mutations that add a base
pair. Three such mutations will add an amino acid. I don't know what
fewer than three will do, but they (and the third one) could be
neutral, harmful, or beneficial. The first two kinds (neutral and
harmful) will tend to be eliminated and not fix in the population.
Even if the mutation is beneficial, after a few amino acids are added
on the end, the shape of the protein will probably change due to
forces involved in protein folding. Thus we will need about as many
changes of shape as their are amino acids added (to within a small
constant factor). If the shape does not change, then the function
will probably not change much, either, which would mean that not much
change in the organism would occur.

When we have a protein with a new shape, the old function will no
longer be performed. This will probably be harmful to the organism.
So in order to allow this, we will have to first copy the gene by a
mutation. This copy will be neutral and probably eliminated, too.
If not, it will be beneficial, so when the shape changes, the mutation
is probably harmful and will be eliminated. Even if not, we will end
up generating a sequence of genes, each differing by only a small
length from the preceding members. This whole scenario is becoming
ridiculous.

Another possibility is to imagine that pieces of existing genes got
shuffled around to produce new genes with beneficial functions in the
cell. A problem with this is that it by definition involves huge
changes in protein shape, not compatible with evolution's gradual
change philosophy. Also, such large changes in structure are very
unlikely to produce anything useful. Finally, such shuffling of
genetic material is likely to be fatal, so it can't happen very
often.

Anyway, how many of these length-increasing mutations can be
beneficial? Note that only about 1 in 1000 of mutations can add an
amino acid on the end. Many mutations will be point mutations, and
some will delete an amino acid. Even of those that add an amino acid,
some will be neutral and some harmful. So if we assume that 1 in 1000
of the length increasing mutations at the end of a gene are
beneficial, it seems a plausible estimate and leads to the same rate
of evolution as mentioned earlier. If anyone has better figures, I
would be happy to have them.

The question is now whether this is an adequate number. For this we
will use the one in 106 probability estimate that a major
mutation will be beneficial; of course, this is undoubtedly much too
generous, and one in 1040 or less is more likely. The
human genome has 3*109 base pairs, and maybe
3*108 are functional. To create this amount of genetic
material, we have to increase the length of a gene about this many
times (to within a factor of 2 at least), and each such increase would
involve a change in shape of the coded protein. This can be avoided
by copying genes and mutating the copies, but I don't think that this
will reduce the number by very much. Now, minor mutations (those that
do not change the shape of the protein) probably don't have much
effect on the organism anyway, so we would expect that most of the
change to the genome was due to major mutations. Thus we only have
106 beneficial major mutations to account for
3*108 functional base pairs (or maybe half this number).
We see that this number is entirely inadequate.

To get around this, we need to increase the population by a factor of
at least 102. This would mean that we probably would not
see many (probably not any) shared pseudogenes or other shared neutral
mutations between different species, depending on how the population
size varied with time. Furthermore, there should at least be some
species (according to accepted evolutionary theory) that have
persisted relatively unchanged for hundreds of millions of years with
huge populations; these should have few, if any, shared pseudogenes
and considerable variation in their non-functional DNA.

What Should Non-Functional DNA Look Like?

We now raise some other questions concerning shared pseudogenes. If
the "non-functional" DNA really has a function, then Edward Max's
argument again disappears. Let's assume that this DNA really has no
function. Then we would expect it to be random. That is, in each
individual, the non-functional DNA would be a random sequence of base
pairs, and for two different individuals, we would not expect their
non-functional DNA to agree any more than would be expected on the
basis of chance. So two unrelated human beings should have about 25
percent agreement in their base pairs in the non-functional DNA. It
would not matter if humans originated 10 million years ago, because
they would have inherited non-functional DNA from ancestors who would
have inherited it from still more distant ancestors. In the billions
of years of evolution, random mutation should have removed all trace
of order in the non-functional DNA. There certainly should not be any
long recognizable patterns in it. I would be interested to know if
this is so. If the non-functional DNA is virtually identical in all
individuals, this means that either this DNA has a function, or that
the origin of man is very recent and all humans started out with the
same non-functional DNA. Edward Max tells me that human DNA sequences
differ between individuals by about one in every 200 base pairs, which
seems to imply that even the non-functional DNA is virtually identical
in all humans.

We now give justification for the statement that the non-functional
DNA should be randomized by mutations, since this is not obvious. For
the sake of illustration, suppose that there is one point mutation per
base pair for every 200 million years. This figure is obtained from
the following quotation from
Introduction to Evolutionary Biology from the talk.origins
archive:

Li and Graur, in their molecular evolution text, give the rates of
evolution for silent vs. replacement rates. The rates were estimated
from sequence comparisons of 30 genes from humans and rodents, which
diverged about 80 million years ago. Silent sites evolved at an
average rate of 4.61 nucleotide substitution per 109
years. Replacement sites evolved much slower at an average rate of
0.85 nucleotide substitutions per 109 years.

Non-functional DNA behaves much like silent sites with respect to
mutations. A rate of 4.61 substitutions per billion years means about
one per 200 million years. Suppose we consider half this many years,
so about half of the base pairs will have mutated during this time.
This would be at most 100 million generations, probably. Let's also
suppose that the population is large enough (significantly larger than
25 million) so that probably none of these mutations will have spread
very far relative to the whole population. Let's assume that at the
beginning, all the non-functional DNA in the population is identical.
We compare two random individuals after 100 million years. Each will
have about half of the non-functional DNA mutated in this time period
(considering only point mutations), actually somewhat less. Thus
one-fourth of the base pairs will be mutated in neither individual,
one-fourth in both individuals, and one-half in one but not the other.
The first one-fourth of base pairs will agree between the two. The
next one-fourth will probably disagree about half of the time if each
mutation spreads to only half the population on the average.
The other half will disagree. So we get about 9/16 disagreement in
the non-functional DNA. As time passes, this figure will get larger
and approach 3/4 since their initial DNA will differ as well.

According to population genetics, if a mutation does spread to the
whole population, it takes on the average about 4N generations to do
so, where the population size is N. However, due to the existence of
partially isolated sub-populations, in reality this should take much
longer than 4N generations. In order to get a significant amount of
disagreement, we argued above that the population must be
significantly larger than 25 million, since point mutations that do
spread to the whole population will probably then take significantly
longer than 100 million generations to do it. However, in fact a
population significantly under 25 million should still suffice for
this argument. This is a reasonable population size. For generation
times of say 10 per year, the population would have to be 10 times
larger.

Now, suppose enough time passes for 1/10 of the DNA to be subject to a
point mutation. This would be 20 million years, or about 20 million
generations. Then we would expect to get about 2/10 disagreement in
non-functional DNA, even if the population started off with identical
DNA. For this, the population would have to be somewhat larger than 5
million. (In fact, a much smaller population size would probably
suffice.) This is still a much larger disagreement than is observed
for humans. Since the generation time would probably be at least 10
years, humans would only need a population of about a million or more
to reach this much disagreement in 20 million years. This seems to be
an evolutionary puzzle, because the observed difference between humans
seems to be about 1 in 200.

We could assume that population bottlenecks occurred during which the
genetic material became uniform. But if this happened, the functional
DNA would also become uniform in the population, except for beneficial
traits that were heterozygous. It is my impression that such
homogeniety is not observed as a rule today. It is difficult to
recover genetic variety in the functional DNA, since it is
tremendously expensive evolutionarily to construct alleles coding for
proteins with new shapes. This is evidence that such extended
bottlenecks did not occur.

The same computations apply to "silent" positions in the coding part
of the DNA. A silent position is a base pair that can be changed
without changing the amino acid coded by the gene. Since such
positions have little or no effect on the organism, they behave much
like non-functional DNA. Suppose a gene has k silent positions, and
suppose the population is large enough so that no mutation is likely
to spread to the whole population in 100 million years. Then in 100
million years, we should expect about half of these positions to have
mutated. Assuming the population is large enough, each silent
position will have about half of its DNA without a mutation and half
of the DNA with a mutation after 100 million years. I estimate that
at least 1/6 of the base pairs in a typical gene would be silent
positions, and maybe as many as 1/3. Thus we should expect at least a
1/12 disagreement in the base pairs between alleles of two random
individuals in the population after 100 million years, not even
counting mutations that change an amino acid. A smaller average
disagreement would indicate a recent origin of life or a severe
extended population bottleneck, but the latter is unlikely to have
occurred in all species in the traditional evolutionary scenario. The
observed value of one difference in 200 base pairs among humans is
significantly under the 1/12 value.

The actual amount of difference between humans is less than
one in 200 base pairs, as the following quotation shows:

"Two genomes chosen from the human population are about 99.8 percent
identical, affirming our common heritage as a species. But the 0.2
percent variation translates into some six million sequence
differences."

This quotation is taken from "Mapping Heredity: Using Probabilistic
Models and Algorithms to Map Genes and Genomes (Part I)," by Eric
S. Lander, Notices of the AMS July 1995. In fact, the average difference
appears to be less than this:

Can DNA typing uniquely identify the source of a sample? Because any
two human genomes differ at about 3 million sites, no two persons
(barring identical twins) have the same DNA sequence. Unique
identification with DNA typing is therefore possible provided that
enough sites of variation are examined.

This is taken from
Chapter 3. DNA Typing: Statistical Basis for Interpretation.
However, we will use the six million figure to be conservative. In
order to get this amount of difference, we only need one mutation per
thousand base pairs since the origin of the human race. Using the
above rate of mutation, and recalling that most of the DNA is thought
to be non-functional, it should only require about 200,000 years for
this amount of difference to arise. This gives an age estimate of
200,000 years for the human race. However, the figure really must be
significantly smaller than this, because there was undoubtedly some
variation at the start, and because the actual rate of mutation is
arguably faster than one per 200 million years. In addition, some
mutations alter many base pairs at the same time.

We now estimate how large the human population must be in order
for this 200,000 year estimate to be valid. A population geneticist
sent me the following information about the propogation of
neutral mutations:

There is a roughly 1/N chance of a new neutral mutation being fixed.
There is a 2/N chance of it getting half way, and it will do so in
roughly half the time (4N/2). Half of these will get the whole way,
and they will take another 4N/2 generations. Better than that
requires a more detailed calculation.

Now, in 200,000 years there would be less than 20,000 generations. A
neutral mutation will spread to the whole population in an average of
20,000 generations if the population size [N] is about 5,000. But if
the population size is about 10,000 or larger, neutral mutations will
on the average spread to only half of the population, which is
sufficient for our age estimage to be valid. The value 10,000 for the
human population is quite small, and it is reasonable to assume that
the human population was generally much larger than this, implying
that our young age estimate is correct. We suspect that a similar
young age estimate is valid for other species as well, which I find
difficult to reconcile with the accepted view of earth's history. For
example, dogs and wolves also seem to have about the same or less
genetic diversity as compared to humans.

There is another mechanism that can reduce this genetic variation, and
this is the following: When a beneficial mutation spreads to the whole
population, it will tend to carry along nearby base pairs, thereby
reducing genetic diversity in its neighborhood. The size of the
neighborhood is related to how fast it spreads. If it spreads to the
whole population in about 1000 generations, then the size of this
neighborhood is about 100,000 base pairs, since crossovers generally
occur once in 100 million base pairs and there would be a thousandfold
multiplication of them in this time. Thus 30,000 such mutations could
essentially eliminate all the genetic diversity in the DNA if they
were evenly spaced throughout the DNA and spread rapidly enough. They
would have to spread in a total of about 400,000 years to produce the
observed low genetic diversity. However, the fact that humans still
have considerable genetic diversity (in blood types, for example)
suggests that this mechanism has not been operating.

Also, having 30,000 such mutations, each with a fitness advantage of
about .01, seems to be a large increase in fitness for a short (in
evolutionary terms) time interval. In fact, .001 seems to be a more
typical value for the selective advantage (according to Simpson,
quoted in Spetner, Not by Chance, page 102), which would require
300,000 such beneficial mutations fixing in 400,000 years, a rather
high rate of evolution. In reality, there would probably have to be
many more than this to guarantee that the whole genome would be
covered, due to their probable irregular distribution. If we assume
one mutation fixing per year and 10 percent functional DNA, this leads
to a rate of mutation of about one substitution per base pair per 300
million years. If we assume one percent functional DNA, this leads to
a mutation rate of about one substitution per base pair per 30 million
years. Both are much faster than assumed by evolutionists for
functional genes, especially the latter rate. This makes such rates
of evolution implausible, and strengthens the case that the human race
(and probably all other species) are young.

Furthermore, many species persist for long (apparent) time periods in
the fossil record with little change. These species do not appear to
be evolving much, so we cannot use this mechanism of beneficial
mutation spread to explain a low genetic diversity in them. Only a
rapidly evolving species can reduce its genetic diversity in this way.
If we try to escape from the dilemma by assuming that the rate of
mutation is very small, explaining the small diversity, then the
assumed evolution of species could not have occurred within the
assumed time spans. The only plausible mechanism that can account for
the data is that the human race experienced a severe population
bottleneck recently which reduced the genetic diversity, or else was
recently created essentially uniform. I suspect that the same
reasoning applies to all other species, too, which seems to be a
puzzle if one is not a creationist. In fact, this conclusion appears
to flatly contradict the fossil record, which shows some species
persisting with large populations for many millions of years. This is
another problem for the standard theory, and suggests that the fossil
record was laid down recently and quickly.

We also note that there is a tremendous difference between the kind of
genetic diversity one would expect due to recent mutations, and that
which is observed. If the existing genetic diversity among humans
arose from recent mutations, then we should expect about 998 of 1000
humans to agree in a given base pair, and only about 2 in 1000 to
differ. This should be true for all base pairs. The real situation
is much different: for many alleles, there are several (or many, for
some species) alleles that are quite common in the population. This
is true for blood type, hair color, eye color, and so on. This seems
to be proof positive that the human species did not reduce its genetic
diversity by rapid evolution, nor did it generate it by recent
mutations. All of these alleles would have had to originate recently
and had a high selective advantage to become common in the population,
yet none had a high enough selective advantage to eliminate the
others. It must be the case, then, that the human race is young (or
else there would be more diversity) and that the observed genetic
diversity existed from the beginning. In fact, a very reasonable
alternative hypothesis is that beneficial mutations are very rare and
have only an insignificant effect on evolution, in most cases, even
over large time periods. The observed changes are then almost all due
to changes in frequencies of existing genetic material. Of course,
this implies creationism.

Now, we discuss the fate of a mutation in the non-functional region of
DNA. This part of the DNA is subject to recombinations (crossovers)
which occur about once per 108 base pairs per meiosis.
This means about 30 per generation for humans. These will tend to
chop the genetic material up into pieces about 108 base
pairs long. With each generation, the number of pieces per chromosome
will increase linearly. If we have one crossover per chromosome per
generation, then after one generation there will be two pieces, after
two generations there will be three pieces, and so on. After a
million generations the pieces will be 108 / 106
or 102 base pairs long on the average, each piece inherited
by a different path. If man and ape separated 10 million years ago,
then a million generations is a reasonable estimate. So we should not
expect to see any piece of a pseudogene that has more than about 100
base pairs in it. Recall also that each pseudogene has only a small
chance of fixing in the population, so that we should only see at most
one piece of the pseudogene altogether.

The LGGLO pseudogene has 3364 base pairs, according to Edward Max.
Thus if it arose all at once in some individual (unlikely), we would
not expect to find more than about 1/30 of it in any human. This
would not agree with the appearance of the whole pseudogene in one
individual, which I believe was reported. It is more realistic to
assume that this was initially a functional gene in all humans, which
would be consistent with its common appearance. However, for
insertions of new (neutral) material, this would not be so. The
farther back one goes, the smaller the pieces should be. For a 20
million generations, the pieces of a pseudogene would be at most a few
base pairs long on the average. This would correspond to possibly 50
million years, not a long period of time by evolutionary standards.
We would never expect to find any common sequence having a hundred
thousand base pairs, even for fairly recent events, unless such
sequences were present in all individuals at some time in the remote
past. This only pushes the problem back further in time, unless this
material was beneficial to the organism at some time. Then it must
have become beneficial to inactivate this genetic material for some
reason, since neutral mutations will not spread, as a rule.
Otherwise, it must be that life originated recently, or that there is
a function for the "junk" DNA. It is also possible that a small
population could lead to uniformity of the DNA.

If any evolutionist has answers to these points, I would most
appreciate hearing from him or her. For example, one individual
writes that single stretches of non-functional DNA will likely spread
to the whole population eventually and in this way make all the
non-functional DNA nearly identical. He feels that crossovers will
not have much of an effect because the two chromosomes that are
crossed over are already almost identical. I'd be interested to learn
if others agree with this.

Here are some initial comments on this reply. It is true that
according to population genetics, non-functional traits (and
non-functional DNA) will eventually spread to the whole population.
The expected time for this is 4N generations when it happens, where N
is the population size. But in reality it should take much longer and
may even be impossible, because one has sub-populations that tend to
interbreed and are to some extent isolated from one another by
geographic and social factors. And while this spread is taking place,
the DNA is subject to being broken up by crossing over
(recombinations). The respondent notes that it is estimated that all
humans have a common paternal ancestor of about 40,000 years. This
would be about 4,000 generations at most. This would correspond to a
population size of about 1,000. But as I said, in reality this is
probably not possible. Also, even if there were a population this
small, due to the superior fitness of humans it would quickly
increase, making such a spread of the Y chromosome unlikely. However,
it is conceivable that a favorable mutation to the Y chromosome could
rapidly spread to a larger population. One could then call the bearer
of this mutation the first true human male. The common female
ancestor is estimated at 200,000 years, which would correspond to
20,000 generations at most and a population size of at most about
5,000 but probably much less as argued above. It is difficult to see
how a favorable mutation could lead to a more rapid spread of common
female ancestry, but it is possible that a mutation to the
mitochondrial DNA could accomplish this. Another plausible
explanation is that at one time the only humans on earth were a man
and a woman and their children, in the not too distant past.

Of course, we note that for evolution to proceed, one needs a large
population size in order to have enough beneficial mutations to spread
to the whole population. So one must have had populations in the
millions (or billions) most of the time, implying a much slower rate
of spread of neutral traits to the whole population and much more time
for mutations and recombinations to enter in while this was
happening.

We also note that some apparently non-functional traits such as being
able to curl one's tongue and maybe blood type and eye color still
show much variability within the human population, despite the
tendency of genetic variability to reduce according to population
genetics. So why should the non-functional DNA be any different? Why
should we not see similar variability in the non-functional DNA?
(The respondent points out that there is actually more variability in the
non-functional DNA than in the functional DNA, though still not much.)
And if these traits (such as eye color) are not neutral, the most
beneficial ones should have won out even faster. In addition, it is a
very strong statement to assert that all the DNA of all humans is very
similar in the non-functional portion. By statistical arguments, we
would expect some of the DNA to spread more slowly and some not to
spread to all the population. To have all of the non-functional DNA
in the whole population essentially identical is really extreme and a
statistical impossibility, unless there was a dramatic population
bottleneck as mentioned above. Since humans are probably not unique
in this, one would have to assume similar bottlenecks for other
species, too. Of course, this is not a problem for the creationist
viewpoint. The other possibility is that this "non-functional" DNA
really has a function.